No clue who to go to without wasting time. My mind opens up 1-3 days after I drink alcohol, I feel enlightened, then I go back to my old self... : Advice

Nobody seems to have any idea, i've posted on multiple forums and threads about this issue.. Doctor first? Psychiatrist, Psyhologist....

Basically here's whats weird about me... Summary at bottom...

Can anyone figure out what's wrong with me? It's so freaking strange.

So basically any night that I drink... I don't even have to get that drunk at all. No matter what the next 1-3 days I feel absolutely ecstatic. Everything in life amuses me. I'm constantly flooded with happy emotions and I become very eloquent and socially aware. I randomly start recalling words I'd never normally use and can form intricate sentences on the fly aswell as holding full fledge intellectual conversations. It's like a plateau that slowly drops off. The first day after its the most intense then the second it's slightly diminished (60%) third day it's 30-40% then fourth day it's kinda there but not really.

Its so strange and I don't know what it is. I want to ALWAYS be like this. I feel like I become the perfect image of myself. It's saddening to slide down the subsequent days after and becoming my normal self. Stuff just doesn't interest me as much and my motivation/curiousity/intellectual ability gets severely reduced aswell as my concentration lowering and happiness (all slightly but noticeable) . Here's a summary of the emotions experienced. Very happy. I go up to random people and be so friendly for no reason at all. Beyond motivated and willing to take on a lot of things. Very well off socially. Mind processes everything 2-3x as fast coming up with complex words and sentence structure/rebuttals.

I can literally go on and on. My mind feels like it finally opens up and I can see the whole picture at once. I'm so confused. Anyone? Also I swear to god I'm not trolling at all. While my friends are moaning on the couch about the night before I'm all over the place wanting to get the day started and pouring my cup of coffee. It's like I'm missing something that should be there and it gets finally released. Maybe along the lines of dopamine receptors? I literally only saw one thread on a drug forum and it was from like 2007 of someone having similar issues. What are my solutions to this? L-Tyrosine? A multi vitamin ? Visiting a doctor? Some obscure nootropic? I swear this isn't all in my head either because even if I forget this happens to me it happens anyway if you get what I mean, people around me have even noticed and commented how it's like talking to a different person. I put no effort in but I can perfectly argue my points with no hesitation and have an insane drive to explore,live and learn to better myself in every way possible. I hope anyone that reads this could input anything.

Tl;dr days after drinking my bodies a lot different and there's subtle but noticeable personality changes (curiousity,motivation, articulateness, altertness)

First: welcome to the club
Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

First: welcome to the club
Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

Hey thanks for the greeting!

More people have this then I expected although everyone's slightly different the general principle is still there. I think I'm going to go to a doctor and see what they say. Also I would like to try piracetam and see what results I recieve.

First: welcome to the club
Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

Hey thanks for the greeting!

More people have this then I expected although everyone's slightly different the general principle is still there. I think I'm going to go to a doctor and see what they say. Also I would like to try piracetam and see what results I recieve.

If forums like these can't find the cause I highly doubt a regular doc can explain it unless it's an expert on alcohol and the brain. But, who knows, let us know if he has something enlightening to say.

First: welcome to the club
Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

Hey thanks for the greeting!

More people have this then I expected although everyone's slightly different the general principle is still there. I think I'm going to go to a doctor and see what they say. Also I would like to try piracetam and see what results I recieve.

If forums like these can't find the cause I highly doubt a regular doc can explain it unless it's an expert on alcohol and the brain. But, who knows, let us know if he has something enlightening to say.

Yeah that's why I feel like i'm going to be wasting my time, I also emailed my doctor from back home maybe she knows.

The brain is highly vulnerable to the neurotoxic effects of alcohol, and cognitive disorders may result from brain damage caused by chronic alcohol abuse.26 The neurotoxic effects of alcohol that cause cognitive deficits may be mediated directly through damage to brain structures or indirectly through malnutrition, metabolite toxicity, electrolyte imbalance, or accompanying physical illnesses including liver disease and infection.27 The direct neurotoxic effect of alcohol is mediated via its action on the NMDA receptors of glutamatergic neurons. Acute alcohol intake exerts an inhibitory effect on NMDA receptors[!]and, thus, induces receptor up-regulation, but when alcohol intake ceases, the up-regulated receptors are no longer inhibited, resulting in an excessive stimulation of NMDA receptors. This, in turn, causes an excessive influx of calcium with cytotoxic effects.26 Glutamatergic neurons are densely concentrated in the frontal lobes and subcortical areas such as the hippocampus, and these brain regions are particularly vulnerable to excitotoxic effects produced by alcohol intake.26 Thiamine deficiency and Korsakoff syndrome resulting from chronic alcohol abuse is an example of indirect alcohol neurotoxicity. Thiamine deficiency causes an excessive release of glutamate which, like alcohol, can exert a neurotoxic effect; in fact, chronic alcohol abuse and thiamine deficiency may have an additive or even synergistic neurotoxic effect.28 Studies of amnesia in patients with Korsakoff syndrome have shown that the condition may have an anterograde component with inability to learn new information, and a retrograde component in which the recent memory is more impaired than remote memory, and a confabulation component associated with these memory defects.29 The apolipoprotein E (APOE) epsilon 4 allele provides a possible genetic explanation for susceptibility to alcohol-induced neurotoxicity. Research findings suggest that people with the allele have a less effective neural repair mechanism and, thus, are more susceptible to the deleterious effects of alcohol.30,31 Elevated serum levels of homocysteine is related to alcoholism,32 and leads to increase of glutamatergic neurotransmission via overstimulation of NMDA receptors.33 This plays a crucial role in the neurobiology of alcoholism, particularly regarding cognitive impairment,34 brain atrophy,35 and alcohol withdrawal seizures.36 Regarding to alcohol neurotoxicity related to immune system, it is reported that chronic alcohol induces systemic cytokines particularly tumor necrosis factor alpha (TNF α). TNF α appears to involve potentiation of glutamate excitotoxicity and activates resident microglia inducing neuroinflammation.37 There are the recent findings in micoglia and astrocyte function toward neurotoxicity via reactive oxygen species under heavy alcohol consumption.37-40 Taken together, alcohol disruption of cytokines and inflammation contribute in multiple ways to a diversity of alcoholic neurotoxicity.

The long-term effect is NMDA upregulation, which also upregulates excitotoxicity. Short-term effects are more difficult to characterize, or less studied with less information in the literature.

Alcohol and Cognition in the Elderly: A Review
The brain is highly vulnerable to the neurotoxic effects of alcohol, and cognitive disorders may result from brain damage caused by chronic alcohol abuse.26 The neurotoxic effects of alcohol that cause cognitive deficits may be mediated directly through damage to brain structures or indirectly through malnutrition, metabolite toxicity, electrolyte imbalance, or accompanying physical illnesses including liver disease and infection.27 The direct neurotoxic effect of alcohol is mediated via its action on the NMDA receptors of glutamatergic neurons. Acute alcohol intake exerts an inhibitory effect on NMDA receptorsand, thus, induces receptor up-regulation, but when alcohol intake ceases, the up-regulated receptors are no longer inhibited, resulting in an excessive stimulation of NMDA receptors. This, in turn, causes an excessive influx of calcium with cytotoxic effects.26 Glutamatergic neurons are densely concentrated in the frontal lobes and subcortical areas such as the hippocampus, and these brain regions are particularly vulnerable to excitotoxic effects produced by alcohol intake.26 Thiamine deficiency and Korsakoff syndrome resulting from chronic alcohol abuse is an example of indirect alcohol neurotoxicity. Thiamine deficiency causes an excessive release of glutamate which, like alcohol, can exert a neurotoxic effect; in fact, chronic alcohol abuse and thiamine deficiency may have an additive or even synergistic neurotoxic effect.28 Studies of amnesia in patients with Korsakoff syndrome have shown that the condition may have an anterograde component with inability to learn new information, and a retrograde component in which the recent memory is more impaired than remote memory, and a confabulation component associated with these memory defects.29 The apolipoprotein E (APOE) epsilon 4 allele provides a possible genetic explanation for susceptibility to alcohol-induced neurotoxicity. Research findings suggest that people with the allele have a less effective neural repair mechanism and, thus, are more susceptible to the deleterious effects of alcohol.30,31 Elevated serum levels of homocysteine is related to alcoholism,32 and leads to increase of glutamatergic neurotransmission via overstimulation of NMDA receptors.33 This plays a crucial role in the neurobiology of alcoholism, particularly regarding cognitive impairment,34 brain atrophy,35 and alcohol withdrawal seizures.36 Regarding to alcohol neurotoxicity related to immune system, it is reported that chronic alcohol induces systemic cytokines particularly tumor necrosis factor alpha (TNF α). TNF α appears to involve potentiation of glutamate excitotoxicity and activates resident microglia inducing neuroinflammation.37 There are the recent findings in micoglia and astrocyte function toward neurotoxicity via reactive oxygen species under heavy alcohol consumption.37-40 Taken together, alcohol disruption of cytokines and inflammation contribute in multiple ways to a diversity of alcoholic neurotoxicity.NMDA receptor-mediated excitotoxicity depends on the coactivation of synaptic and extrasynaptic receptors.
N-methyl-D-aspartate receptors (NMDAR) overactivation is linked to neurodegeneration. The current prevailing theory suggests that synaptic and extrasynaptic NMDAR (syn- and ex-NMDAR) impose counteracting effects on cell fate, and neuronal cell death is mainly mediated by the activation of ex-NMDAR. However, several lines of evidence implicate the limitation of this theory. Here, we demonstrate that activation of NMDAR bi-directionally regulated cell fate through stimulating pro-survival or pro-death signaling. While low-dose NMDA preferentially activated syn-NMDAR and stimulated the extracellular signal-regulated kinase ½-cAMP responsive element-binding protein-brain-derived neurotrophic factor pro-survival signaling, higher doses progressively activated increasing amount of ex-NMDAR along with syn-NMDAR and triggered cell death program. Interestingly, the activation of syn- or ex-NMDAR alone did not cause measurable cell death. Consistently, activation of syn- or ex-NMDAR alone stimulated pro-survival but not pro-death signaling. Next, we found that memantine, which was previously identified as an ex-NMDAR blocker, inhibited intracellular signaling mediated by syn- or ex-NMDAR. Simultaneous blockade of syn- and ex-NMDAR by memantine dose-dependently attenuated NMDAR-mediated death. Moreover, long- but not short-term treatment with high-dose NMDA or oxygen-glucose deprivation triggered cell death and suppressed pro-survival signaling. These data implicate that activation of syn- or ex-NMDAR alone is not neurotoxic. The degree of excitotoxicity depends on the magnitude and duration of syn- and ex-NMDAR coactivation. Finally, genome-wide examination demonstrated that the activation of syn- and ex-NMDAR lead to significant overlapping rather than counteracting transcriptional responses.

Selective mGluR5 antagonists MPEP and SIB-1893 decrease NMDA or glutamate-mediated neuronal toxicity through actions that reflect NMDA receptor antagonism
1. The metabotropic glutamate receptors (mGluRs) are a family of G-protein linked receptors that can be divided into three groups (group I, II and III). A number of studies have implicated group I mGluR activation in acute neuronal injury, but until recently it was not possible to pharmacologically differentiate the roles of the two individual subunits (mGluR1 and mGluR5) in this group. 2. We investigated the role of mGluR5 in acute NMDA and glutamate mediated neurodegeneration in cultured rat cortical cells using the mGluR5 antagonists MPEP and SIB-1893, and found that they provide significant protection at concentrations of 20 or 200 microM. 3. These compounds act as effective mGluR5 antagonists in our cell culture system, as indicated by the ability of SIB-1893 to prevent phosphoinositol hydrolysis induced by the specific mGluR5 agonist, (RS)-2-chloro-5-hydroxyphenylglycine (CHPG). 4. However, they also significantly reduce NMDA evoked current recorded from whole cells voltage clamped at -60 mV, and significantly decrease the duration of opening of NMDA channels recorded in the outside out patch configuration. 5. This suggests that although MPEP and SIB-1893 are effective mGluR5 antagonists, they also act as noncompetitive NMDA receptor antagonists. Therefore, the neuroprotective effects of these compounds are most likely mediated through their NMDA receptor antagonistaction, and caution should be exercised when drawing conclusions about the roles of mGluR5 based on their use.

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"Lithium has some mGluR5 antagonist effects and has also been utilized in the Drosophila model and in the KO mouse with effects similar to MPEP (McBride 2005, Yan 2005)"
"Lithium also down-regulates the mGluR5 system, and an open trial of lithium in individuals with FXS [fragile X] demonstrated positive behavioral effects, with some signs of improved cognition as well (Berry-Kravis 2008)"

Short-term effects I suspect are a kind of "afterglow", mediated by the same mechanisms.

Gone fishing on wiki for clues, and I found:

Ethanol inhibits the ability of glutamate to open the cation channel associated with the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. Stimulated areas include thecortex, hippocampus and nucleus accumbens, which are responsible for thinking and pleasure seeking. Another one of alcohol's agreeable effects is body relaxation, possibly caused by neurons transmitting electrical signals in an alpha waves-pattern; such waves are observed (with the aid of EEGs) when the body is relaxed.[citation needed]

Areas of the brain responsible for planning and motor learning are sharpened. A related effect, caused by even low levels of alcohol, is the tendency for people to become more animated in speech and movement. This is due to increased metabolism in areas of the brain associated with movement, such as thenigrostriatal pathway. This causes reward systems in the brain to become more active, which may induce certain individuals to behave in an uncharacteristically loud and cheerful manner.

So having run out of patience... my bes guess is that in those areas an increase in LTP, ATP turnover, neuromodulation, synaptic transmission, or growth related factors. Any of these mechanisms could in part explain the association between light drinking and improved cognition. Further investigation is warranted.

Moderate alcohol consumption and cognitive risk.
We reviewed 143 papers that described the relationship between moderate drinking of alcohol and some aspect of cognition. Two types of papers were found: (1) those that provided ratios of risk between drinkers and nondrinkers (74 papers in total) and (2) those that, although they did not provide such ratios, allowed cognition in drinkers to be rated as "better," "no different," or "worse" than cognition in nondrinkers (69 papers in total). The history of research on moderate drinking and cognition can be divided into two eras: 1977-1997 and 1998-present. Phase I (1977-1997) was the era of neuropsychological evaluation involving mostly young to middle-aged (18-50 years old) subjects. Although initial studies indicated moderate drinking impaired cognition, many later studies failed to confirm this, instead finding no difference in cognition between drinkers and nondrinkers. Phase II (1998-present) was and is the era of mental status exam evaluation involving mostly older (≥55 years old) subjects. These studies overwhelmingly found that moderate drinking either reduced or had no effect on the risk of dementia or cognitive impairment. When all the ratios of risk from all the studies in phase II providing such ratios are entered into a comprehensive meta-analysis, the average ratio of risk for cognitive risk (dementia or cognitive impairment/decline) associated with moderate "social" (not alcoholic) drinking of alcohol is 0.77, with nondrinkers as the reference group. The benefit of moderate drinking applied to all forms of dementia (dementia unspecified, Alzheimer's disease, and vascular dementia) and to cognitive impairment (low test scores), but no significant benefit against cognitive decline (rate of decline in test scores) was found. Both light and moderate drinking provided a similar benefit, but heavy drinking was associated with nonsignificantly higher cognitive risk for dementia and cognitive impairment. Although the meta-analysis also indicated that wine was better than beer or spirits, this was based on a relatively small number of studies because most studies did not distinguish among these different types of alcohol. Furthermore, a number of the studies that did make the distinction reported no difference among the effects of these different types of alcohol. Therefore, at present this question remains unanswered. Analysis also showed that the presence of the apolipoprotein E epsilon 4 allele eliminated the benefit of moderate drinking. However, this was based on a relatively small number of studies and several other studies have found a beneficial effect of the epsilon e4 allele. Further studies are necessary to settle this question. The benefit of moderate alcohol for cognition was seen in both men and women, although the amount and pattern of drinking is very different between the two sexes. Lastly, the finding of unaffected or significantly reduced cognitive risk in light to moderate drinkers was seen in 14/19 countries for which country-specific ratio data were available, with three of the five remaining countries showing nonsignificant reductions as well. Overall, light to moderate drinking does not appear to impair cognition in younger subjects and actually seems to reduce the risk of dementia and cognitive decline in older subjects.

Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

Actually, somebody did come up with a rational theory and solution for this phenomenon, although it has mixed success amongst others. It was essentially about dopamine dysregulation, and said user reckoned he worked out which dopamine creating system was off, and managed to rectify it...

Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

Actually, somebody did come up with a rational theory and solution for this phenomenon, although it has mixed success amongst others. It was essentially about dopamine dysregulation, and said user reckoned he worked out which dopamine creating system was off, and managed to rectify it...

On the dopamine deficiency, it makes sense, but alcohol's effect here may be very weak, and the whole idea far-fetched. What alcohol would do is release dopamine, downregulate autoreceptors, and thereby further facilitate a dopamine release, which would finally affect a renormalization of postsynaptic receptor levels. On a much stronger level, this is how SSRIs act: by increasing serotonin and decreasing autoreceptors and receptors.

it seems that I am this way with kratom dosent really do much for me but a few days after i take it Im super calm, maybe it builds up but I know this stuff has a half life so really shouldnt be in my system after a while.

it seems that I am this way with kratom dosent really do much for me but a few days after i take it Im super calm, maybe it builds up but I know this stuff has a half life so really shouldnt be in my system after a while.

You're like that with only Kratom? That's strange what about other anxiety reducing supplements?

Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

Actually, somebody did come up with a rational theory and solution for this phenomenon, although it has mixed success amongst others. It was essentially about dopamine dysregulation, and said user reckoned he worked out which dopamine creating system was off, and managed to rectify it...

Yeah I've read this thread, truly interesting and we are very similar but I don't have every effect the same i'm not normally disfunctional throughout the day my mind is just average and okay wheras he had a complete downturn in his emotions etc. Here is what I replied ..

The thing about me is that throughout the days and weeks I'll be normal. Just a stable person with nothing noticeable about them, maybe more social then most people. I get slight anxiety and depression at random times throughout the year. But the one thing I lack is any sort of motivation. Growing up I was filled with ideas, always working on something new. Now I just feel clouded in a light brain fog that never truly allows me to reach my full potential. I can't describe it at all.

Anyways, everything gets reversed the day after drinking like other posters have stated. But to me I highly doubt I have any sort of mutation in those genes, I just feel like I have a lack of dopamine upregulation...

As stated from my other forum post,

I'll wake up from let's say a party with all my other friends they'll be dreading waking up and I will already be so happy just walking around and ready to take on the day (VERY UNUSUAL)

From there my verbal fluency increases tenfold, creating and sustaining a very intelligent conversation I otherwise never would. I don't get where it comes from, I actually give people the attention of day and want/am interested in them. I feel like I build meaningful connections and I honestly blew my parents away because of how deep our conversations were going. I never really care about conversations and just reply in pretty simple sentences but after drinking I actually want to keep a discussion going. I feel like I become a perfect image of myself.

Now onto motivation, I will think of something and without thinking execute the task. I would always struggle to do anything. It's so strange. Everything interests me, I have a sudden appreciation for the world around me and start notice the smaller things and cherish it.... From this new found motivation and my new cognition of formulating amazing ideas and thoughts my productivity sky rockets it's amazing. I can literally go on and on. My mind feels like it finally opens up and I can see the whole picture at once. I'm so confused.

And then the days after it crashes and i'm back to the start.

I honestly am scared to mess around with Nootropics due to me only being 19. It's scary to me messing with my brain while it is still developing so I have just stuck with L-Theanine.

On the dopamine deficiency, it makes sense, but alcohol's effect here may be very weak, and the whole idea far-fetched. What alcohol would do is release dopamine, downregulate autoreceptors, and thereby further facilitate a dopamine release, which would finally affect a renormalization of postsynaptic receptor levels. On a much stronger level, this is how SSRIs act: by increasing serotonin and decreasing autoreceptors and receptors.

Also holy shit I finally got the time to disect your post and spend a while researching. I totally feel like you're going in the right direction. Going to build off of it and see the neuroscience department of my university for clues. It's so interesting and I wonder if this is it? I'm going to look for correlations and start experimenting with Glutamate and GABA receptors as well as present this kind of information to my doctor and wonder what she will say.

Thanks so much for taking the time to look this up and helping me it totally helped me understand the process a lot more better. THANK YOU.

it seems that I am this way with kratom dosent really do much for me but a few days after i take it Im super calm, maybe it builds up but I know this stuff has a half life so really shouldnt be in my system after a while.

You're like that with only Kratom? That's strange what about other anxiety reducing supplements?

Kratom does this a bit, phenibut sometimes as well. I don't see much when I take these things but the next day ill be a little more calm same thing with alcohol but with alcohol i actually get results when I'm actually using it. So my alcohol hangover is a slow moving chill feeling for me..

I chalked it up as being high anxiety person and my nerves basically being dilated a little.

Kratom does this a bit, phenibut sometimes as well. I don't see much when I take these things but the next day ill be a little more calm same thing with alcohol but with alcohol i actually get results when I'm actually using it. So my alcohol hangover is a slow moving chill feeling for me..

I chalked it up as being high anxiety person and my nerves basically being dilated a little.

Interesting. If you do end up finding out a cure don't forget to message me. :D

I will, you know what wrks very well actually having a social circle. I just started taking noopept and I didn't like it at all. I only took it once so cant really go into too much detail it just made me feel very weird. I have trying Ashwaghanda now. PM me if need be.

Update: My doctor prescribed me Cipralex. She thinks I have an underlying anxiety. So stranged because I don't feel that way at all. Since i've taken it I've felt pretty tired and drowsy throughout the day, no changes yet but it should take 2 weeks to fully take effect.

Alcohol, if taken in the evening, changes the architecture of your sleep (the different sleep phases, their frequency, the brain wave density etc). It decreases REM sleep, which is thought to be increased in depressed people. This also seems to be causative, as depriving depressed people of REM sleep temporarily strongly reduces their depression. REM deprivation is just waking somebody up at about 3-4am (as there are more frequent, denser REM episodes in the last half of the night). Of course you do need a full night's sleep (plus your body redoubles REM when you do get back to sleep) so it is not sustainable.

However, it is a very interesting and simple experiment to try and see if it gives you the same feeling as alcohol did.

You can test this further by taking a sleep dose of benadryl tonight, or getting a few days of those non-benzo Z-drugs. They also reduce REM sleep. As do most antidepressants, actually; that could even be their main mechanism of action, not the "increase serotonin" stuff that has been debunked since their first human trials. You know that logic is from drug commercials, right? No psychiatrist actually believes anybody is "deficient in serotonin"; they give out the antidepressants as a drug with an unknown mechanism of action (like many other drugs in medical use).

None of those are sustainable either, but if you need an occasional pick-me-up, it has got to be better than getting drunk.

_____________________________________________________________

however, I can't find decent studies on the magnitude of specifically alcoholic REM suppression in depressed people. What is known, is that alcohol increases the slow wave sleep by a lot in healthy people, even if their REM suppression isn't as significant. That slow wave sleep is substituted for lighter non-REM sleep stages. Plus, REM suppression in healthy people isn't particularly therapeutic, even harmful.

I have the exact same experience, a quick question for my own personal curiosity. Do you find that your a happy drunk ( as opposed to the usual angry drunk ) also do you find that alcohol stimulates you more than makes you drowsy?

For the longest time I was under the assumtion that it was alcohol raising my GABA levels, as I believed i was low in said neurotransmitters. But now im a little less convienced.

The only other two times I get this similar effect is from sleep deprivation( slightly compared to alcohol ), and taking a extremely low dose of LSD. Such as 1/10 what people take to use as a intensive drug.

another theory I have could be that its when certain parts of my brain are locked in to certain ways of thinking that its impossible for it to make connections at a instantly quick way, but when under the influence of alcohol, sleep deprivation oy lsd. Then my brain gets more cloudly and less sure of where the connection should be coming from, so.. basically at that point my brain starts making connections at other less common places.

Just a theory and obviously dumbed down ^

Also this for me is the exact same

I'll wake up from let's say a party with all my other friends they'll be dreading waking up and I will already be so happy just walking around and ready to take on the day (VERY UNUSUAL)

From there my verbal fluency increases tenfold, creating and sustaining a very intelligent conversation I otherwise never would. I don't get where it comes from, I actually give people the attention of day and want/am interested in them. I feel like I build meaningful connections and I honestly blew my parents away because of how deep our conversations were going. I never really care about conversations and just reply in pretty simple sentences but after drinking I actually want to keep a discussion going. I feel like I become a perfect image of myself.

I'm 21 years old and have drunk many many times on the regular and I almost never get Hung over. ^

But I would recommend a micro dose of lsd to see if that helps, because for me its similar effect but better. Makes me a little jittery though.

I'm a very happy drunk and always the life of the party in a social sense. I always have a lot of energy and pump people up to have fun so it really does stimulate me.

In regards to your theories I do see where you're going with those thoughts. I do notice a slightly similar trend with sleep deprivation but not as bad. I have never taken LSD so unfortunately I have not yet tested that theory.

I'm going to get off these anti-depressants because all they've been doing is clouding my mind and making me more of a robot emotionally.

I don't tolerate alcohol at all, get bad headache and hangover from small amounts, but I have the same afterglow from dissociatives / NMDA antagonists and part of ethanol's pharmacology involves NMDA negative modulation too ... interesting thing is that ketamine has been shown to induce kind of a hyper-glutamatergic state somehow, possibly because it antagonises auto receptors and thus makes the processing more effective and also potentially causes a shift from NMDA towards increased AMPA signalling, which might be favourable for long term potentiation and such.

Yeah I've read this thread, truly interesting and we are very similar but I don't have every effect the same i'm not normally disfunctional throughout the day my mind is just average and okay wheras he had a complete downturn in his emotions etc. Here is what I replied ..

Second: we tried to break down this phenomenon in another thread similar to what you've found but unfortunately no one really could explain or recreate this feeling of well-being you, me and others experience.

Actually, somebody did come up with a rational theory and solution for this phenomenon, although it has mixed success amongst others. It was essentially about dopamine dysregulation, and said user reckoned he worked out which dopamine creating system was off, and managed to rectify it...

The thing about me is that throughout the days and weeks I'll be normal. Just a stable person with nothing noticeable about them, maybe more social then most people. I get slight anxiety and depression at random times throughout the year. But the one thing I lack is any sort of motivation. Growing up I was filled with ideas, always working on something new. Now I just feel clouded in a light brain fog that never truly allows me to reach my full potential. I can't describe it at all.

Anyways, everything gets reversed the day after drinking like other posters have stated. But to me I highly doubt I have any sort of mutation in those genes, I just feel like I have a lack of dopamine upregulation...

As stated from my other forum post,

I'll wake up from let's say a party with all my other friends they'll be dreading waking up and I will already be so happy just walking around and ready to take on the day (VERY UNUSUAL)

From there my verbal fluency increases tenfold, creating and sustaining a very intelligent conversation I otherwise never would. I don't get where it comes from, I actually give people the attention of day and want/am interested in them. I feel like I build meaningful connections and I honestly blew my parents away because of how deep our conversations were going. I never really care about conversations and just reply in pretty simple sentences but after drinking I actually want to keep a discussion going. I feel like I become a perfect image of myself.

Now onto motivation, I will think of something and without thinking execute the task. I would always struggle to do anything. It's so strange. Everything interests me, I have a sudden appreciation for the world around me and start notice the smaller things and cherish it.... From this new found motivation and my new cognition of formulating amazing ideas and thoughts my productivity sky rockets it's amazing. I can literally go on and on. My mind feels like it finally opens up and I can see the whole picture at once. I'm so confused.

And then the days after it crashes and i'm back to the start.

I honestly am scared to mess around with Nootropics due to me only being 19. It's scary to me messing with my brain while it is still developing so I have just stuck with L-Theanine.

Unfortunately, you may be the person we're waiting for. It's either a dysfunction and a correction, or normalcy and an enhancement. That both cases now seem to exist implies that it is normalcy and an enhancement, only that you are more at piece with your normal state.